Lanreotide Reduces Liver Volume, But Might Not Improve Muscle Wasting or Weight Loss, in Patients With Symptomatic Polycystic Liver Disease

Temmerman, Frederik; Ho, Thien Ahn; Vanslembrouck, Ragna; Coudyzer, Walter; Billen, Jaak; Dobbels, Fabienne; Pelt, Jos van; Bammens, Bert; Pirson, Yves; Nevens, Frederik

doi:10.1016/j.cgh.2015.05.039

Cited by 31 publications

(29 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By contrast, another study showed that 1-year treatment with octreotide reduces the TLV (-4.95%), but this effect was not significant after 1 additional year of treatment (-0.77%) [32] . In line with this, lanreotide treatment was also reported to have the greatest effects in the first 6 months of administration [31,34] . Furthermore, treatment continuation for 12 additional months did not have any substantial effect in liver volume reduction [34] .…”

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 66%

“…In line with this, lanreotide treatment was also reported to have the greatest effects in the first 6 months of administration [31,34] . Furthermore, treatment continuation for 12 additional months did not have any substantial effect in liver volume reduction [34] .…”

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 66%

“…They bind to somatostatin receptors (SSTRs) localized at the plasma membrane of cholangiocytes and repress adenylate cyclase activity and thus cAMP synthesis. Different studies have reported beneficial effects of the chronic administration of somatostatin analogs in animal models and patients with PLD [18,[26][27][28][29][30][31][32][33][34] . Administration of octreotide (somatostain analog that preferentially binds to SSTR2) to PCK rats resulted in the reduction of liver weight, cyst volume, hepatic fibrosis and proliferation [18] .…”

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 99%

“…However, this effect is not further sustained when extending the therapy for 2 or 4 years with octreotide [32,33] . Importantly, somatostatin analogues display different side effects including injection site pain, bruising and granuloma formation, severe abdominal cramps, diarrhoea, steatorrhea, flatulence or gallbladder stones [30,33,34] .…”

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 99%

See 3 more Smart Citations

Bile Acids in Polycystic Liver Diseases: Triggers of Disease Progression and Potential Solution for Treatment

Labiano¹,

Esparza-Baquer²,

Marzioni³

et al. 2017

Dig Dis

View full text Add to dashboard Cite

Polycystic liver diseases (PLDs) are a group of genetic hereditary cholangiopathies characterized by the development and progressive growth of cysts in the liver, which are the main cause of morbidity. Current therapies are based on surgical procedures and pharmacological strategies, which show short-term and modest beneficial effects. Therefore, the determination of the molecular mechanisms of pathogenesis appears to be crucial in order to find new potential targets for pharmacological therapy. Ductal plate malformation during embryogenesis and abnormal cystic cholangiocyte growth and secretion are some of the key mechanisms involved in the pathogenesis of PLDs. However, the discovery of the presence of bile acids in the fluid collected from human cysts and the intrahepatic accumulation of cytotoxic bile acids in an animal model of PLD (i.e. polycystic kidney (PCK) rat) suggest a potential role of impaired bile acid homeostasis in the pathogenesis of these diseases. On the other hand, ursodeoxycholic acid (UDCA) has emerged as a new potential therapeutic tool for PLDs by promoting the inhibition of cystic cholangiocyte growth in both PCK rats and highly symptomatic patients with autosomal dominant polycystic kidney disease (ADPKD: most common type of PLD), and improving symptoms. Chronic treatment with UDCA normalizes the decreased intracellular calcium levels in ADPKD human cholangiocytes in vitro, which results in the reduction of their baseline-stimulated proliferation. Moreover, UDCA decreases the liver concentration of cytotoxic bile acids in PCK rats and the bile acid-dependent enhanced proliferation of cystic cholangiocytes. Here, the role of bile acids in the pathogenesis of PLDs and the potential therapeutic value of UDCA for the treatment of these diseases are reviewed and future lines of investigation in this field are proposed.

show abstract

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 66%

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 66%

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 99%

Section: Camp and Ca 2+ Signalling In Pldsmentioning

confidence: 99%

See 2 more Smart Citations

Bile Acids in Polycystic Liver Diseases: Triggers of Disease Progression and Potential Solution for Treatment

Labiano¹,

Esparza-Baquer²,

Marzioni³

et al. 2017

Dig Dis

View full text Add to dashboard Cite

show abstract

“…17 In addition, two other nonplacebo controlled clinical trials showed beneficial effects of somatostatin analogs in PLD. 18, 19 Thus, based on these studies, it is reasonable to conclude that : (i) treatment with somatostatin analogs for 6–12 months decreases total liver volume; (ii) reduction in liver volume is sustained beyond 12 month of therapy; (iii) response to treatment varies among patients with some (~15%) non responders; (iv) once therapy is stopped, liver volume starts to increase toward baseline suggesting that long term continuous or intermittent treatment is required; (vi) somatostatin analogs are well tolerated and improve quality of life; and (vii) similar changes in liver volume in response to treatment occurs in patients with ADPKD-associated PLD or isolated ADPLD.…”

mentioning

confidence: 99%